03.2019 | THE SCIENTIST 37erial from cell to cell, says Jason Shepherd, a neuroscientist at
the University of Utah and coauthor of one of the studies. The
genes encoding the vesicles could possibly be holdovers from
past infections, he suggests, and these virus-mimicking cap-
sids could be harboring toxic proteins, such as amyloid β, and
spreading them throughout the brain.
“Clearly, viruses influence the brain,” Shepherd says, but the
nature of that relationship remains unclear.
Forgetfulness lingers
One challenge in understanding how the brain responds to viral
infection is that the effects can linger long after our immune sys-
tem has cleared the infection from our bodies. Earlier this year,
for example, Martin Korte at the Technische Universität Braun-
schweig in Germany and colleagues reported that the brains of
mice infected with certain strains of the flu virus suffered mem-
ory deficits even after they’d seemingly recovered. It turned out
that their brains were full of microglia even 30 to 60 days after
infection first took hold.^14 The microglia levels can start to return
to the normal range around 60 days post infection, with the neu-
rons in the young mice recovering completely, along with the
animals’ memory performance. Still, the microglia numbers can
stay elevated for up to 120 days, Korte tells The Scientist; that’s
equivalent to more than 10 years in human time.
Va n den Pol says such a lag is exactly why scientists have trou-
ble accepting that viruses could cause neurodegenerative diseases.
“In science we often think of some cause and effect being often
milliseconds,” he says. “Here, you’re talking about decades. The
virus goes in and then maybe decades later it can cause some
potentially serious neurodegeneration”—such a long-term link is
hard to demonstrate.
If the connection between viral infections and neurological
problems can be more concretely established, researchers may be
able to develop ways to mitigate the neurological effects, van den
Pol says. Understanding how infections trigger the immune system,
for example, could lead to ways to downregulate glia-driven inflam-
mation in hopes of preventing long-term damage, he suggests.
In the meantime, Smeyne notes that vaccination for
the flu—or at the very least, taking Tamiflu if a person gets
infected—might help prevent neurological complications of
influenza infection. He and his colleagues tested this approach
in mice after their results revealed the link between flu, the
MPTP toxin, and Parkinson’s disease. The team gave a group
of mice an H1N1 vaccine 30 days before infecting the animals
with the virus. Another group of mice were treated with Tami-
flu for the week after they were infected. Both groups of mice
were allowed to recover before being given a low dose of MPTP.
While control mice that did not receive either the vaccine or
flu treatment developed Parkinson’s-like symptoms, treated
mice developed no neurodegenerative effects. “We had pro-
tected against [Parkinson’s-like symptoms] just by early treat-
ment or prophylactic treatment with the vaccine,” Smeyne says.
It’s further evidence to support the idea that viral infections
can damage the brain, Smeyne says, but there’s still no slam-
dunk study that demonstrates a virus can cause Parkinson’s, or
Alzheimer’s, or any number of other neurological disorders. “I do
like the idea that viruses can cause a lot of different brain diseases
as a hypothesis,” van den Pol says. “But I also respect the fact that
it really is a hypothesis.” gReferences- H. Jang et al., “Highly pathogenic H5N1 influenza virus can enter the central
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In science we often think of
some cause and effect being often
milliseconds. Here, you’re talking
about decades.
—Anthony van den Pol, Yale University